Biology and biomedicine · Paper · March 2021
Observing the Genetic Difference of alternative spliced multiple myeloma cells with dose-escalation Tunicamycin
Tunicamycin is a commonly used drug to cause an unfolded protein response in multiple myeloma cells in order to treat the cancer. However, many multiple myeloma cell lines have slowly developed resistance to this treatment. The goal of my project is to find out the reasons in the RNA behind why this resistance is caused, in order to create a better, altered treatment that could possibly circumvent these problems. First, multiple myeloma cells were treated with tunicamycin repeatedly four times, such that the living cells would sufficiently have developed resistance to the treatment. Then a short-term treatment was performed before plating the cells, dividing the cells into a control and treated group to find differences between their RNA to find indicators that cause the resistance. After plating the cells and isolating the RNA, a mass transcriptome analysis returned exonic data to allow us to look at how the resistance was being developed through the creation of proteins and certain protein responses. Upon looking at the data, several markers were made clear, such as the suppression of VAPA and DDIT3 as examples. Through looking at all of these gene markers, the treatment can be slightly altered in order to prevent the suppression of certain responses that would cause the cancer cell to die, thus making the treatment apply to a wider range of cells.